THE EFFECT OF IODIDE INGESTION ON THE DEVELOPMENT OF SPONTANEOUS LYMPHOCYTIC THYROIDITIS IN THE DIABETES-PRONE BB/W RAT

THE EFFECT OF IODIDE INGESTION ON THE DEVELOPMENT OF SPONTANEOUS LYMPHOCYTIC THYROIDITIS IN THE DIABETES-PRONE BB/W RAT
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DOI:
10.1210/endo-118-5-1977
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发表时间:
1986-05-01
期刊:
影响因子:
4.8
通讯作者:
BRAVERMAN, LE
BRAVERMAN, LE
中科院分区:
医学2区
文献类型:
--
作者:
ALLEN, EM;APPEL, MC;BRAVERMAN, LE

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有人认为,高碘摄入会增加桥本甲状腺炎的发病率。糖尿病易感BB/W大鼠在60 - 120日龄之间发生自发性组织学自身免疫性淋巴细胞性甲状腺炎(LT),无功能性甲状腺功能减退。进行研究以确定BB/W大鼠的碘化物给药是否会影响LT的发生率和严重程度并诱导甲状腺功能减退。对42只10月龄BB/W大鼠和71只30日龄BB/W大鼠随意给予碘化物(0.05%水溶液)或自来水(C),持续8周。为了对照目的,还向42只30日龄非糖尿病和非LT倾向BB/W遗传等效大鼠(W系)随意给予0.05%碘化物或自来水(C)12周,并向41只21日龄Wistar大鼠随意给予7周。在一项单独的实验中,断奶BB/W大鼠随意喂食低碘饲料、对照碘充足(C)饲料或Purina食物(P)和自来水8周。在每项实验中,在死亡时采集血液,用于测量血清T4、T3、TSH和抗甲状腺球蛋白抗体(抗Tg Ab),并取出甲状腺进行组织学评价(0 =无LT; 1-4 = LT)。在30日龄BB/W大鼠中,碘剂给药(0.05%)诱导LT发生率显著增加(I,77%; C,30%,P <0.001)。甲状腺重量和血清T4,T3和抗Tg抗体浓度不受碘化物管理。然而,LT的存在与甲状腺重量和抗Tg Ab浓度的显著增加相关。BB/W大鼠低碘饮食组LT发生率明显降低(低碘组8.6%; C组47.3%; P < 0.01),但抗Tg抗体水平无显著性差异。增加碘摄入量并没有显着影响LT的发病率在成年BB/W大鼠,并没有诱导LT或影响甲状腺功能在W系或Wistar大鼠。这些数据表明,碘摄入量显着影响自发LT的年轻,遗传易感大鼠的发病率。
It has been suggested that the incidence of Hashimoto''s thyroiditis is increased in the presence of high iodide intake. The diabetes-prone BB/W rat develops spontaneous histological autoimmune lymphocytic thyroiditis (LT) without functional hypothyroidism between 60 and 120 days of age. Studies were carried out to determine whether iodide administration of BB/W rats would affect the incidence and severity of LT and induce hypothroidism. Iodide (0.05% in water) or tap water (C) was administered ad libitum to 42 10-month-old BB/W rats and 71 30-day-old BB/W rats for 8 weeks. For control purpose, 0.05% iodide or tap water (C) was also administered ad libitum to 42 30-day-old nondiabetic and non-LT-prone BB/W genetically equivalent rats (W-line) for 12 weeks and 41 21-day-old Wistar rats for 7 weeks. In a separate experiment, weanling BB/W rats were fed a low iodine diet, a control iodine-sufficient (C) diet, or Purina chow (P) and tap water ad libitum for 8 weeks. In each experiment, blood was obtained at the time of death for the measurement of serum T4, T3, TSH, and antithyroglobulin antibody (anti-Tg Ab), and the thryoids were removed for histoloigical evaluation (0 = no LT; 1-4 = LT). Iodide adminstration (0.05%) induced a significant increase in the incidence of LT in 30-day-old BB/W rats (I, 77%; C, 30%, P < .001). Thyroid weight and serum T4, T3, and anti-Tg Ab concentrations were not affected by iodide administration. However, the presence of LT was associated with a significant increase in thyroid weight and anti-Tg Ab concentrations. BB/W rats subjected to a low iodine diet exhibited a significantly decreased incidence of LT (low I, 8.6%; C, 47.3%; P < 0.01), but no statistically significant difference in anti-Tg Ab levels. Increased iodide intake did not significantly affect the incidence of LT in adult BB/W rats and did not induce LT or affect thyroid function in W-line or Wistar rats. These data show that iodine intake significantly affects the incidence of spontaneous LT in young, genetically predisposed rats.